Inhibition of glucuronidation in pancreatic cancer improves gemcitabine anticancer activity  

作　　者：Nicolas Alejandro Fraunhoffer Analía Meilerman Abuelafia Brice Chanez Martin Bigonnet Odile Gayet Julie Roques Eduardo Chuluyan Nelson Dusetti Juan Iovanna 

机构地区：[1]Cancer Research Center of Marseille,Inserm,Paoli-Calmettes Institut,Aix-Marseille University,Scientific and Technological Park of Luminy,Marseille 13288,France [2]Buenos Aires University,Center for Pharmacological and Botanical Studies,Faculty of Medicine,National Council for Scientific and Technical Research,Buenos Aires,C1121ABG,Argentina [3]Buenos Aires University,Faculty of Medicine,Department of Microbiology,Parasitology and Immunology,Buenos Aires C1121ABG,Argentina [4]Predicting Med,Scientific and Technological Park of Luminy,Marseille 13288,France

出　　处：《Cancer Communications》2022年第11期1212-1216,共5页癌症通讯（英文）

基　　金：supported by the National Cancer Institute(Grants number 2018-078,2019-037, 2018-079),Canceropole Provence-Alpes-Côte d’Azur,Amidex Foundation and the national institute of health and medical research.

摘　　要：Dear Editor,Pancreatic ductal adenocarcinoma(PDAC)treatment is focused on two regimens.The polychemotherapy,FOLFIRINOX(folinic acid,fluorouracil,irinotecan,oxali-platin),is used in patients with good health conditions[1],while gemcitabine,as monotherapy,in patients with poor health conditions[2–4].Gemcitabine resistance-associated pathways have been targeted to sensitize cancer cells,but the results were disappointing.Using a transcrip-tomic bioinformatics analysis combined with biological validation,we showed that glucuronidation was associ-ated with the gemcitabine resistance in PDAC,and its inhibition could switch tumors from resistant to sensitive.

关 键 词：GEMCITABINE cancer CHEMOTHERAPY 

分 类 号：R735.9[医药卫生—肿瘤]